Volume 2 · Nº 2 Supl · May 2010
There is no universally accepted definition of osteoporosis. One of the most convincing is that proposed by the NIH in 19931, according to which osteoporosis is a generalised disease of the skeleton, characterised by a reduction in bone mass and a deterioration in the microarchitecture of the bone, which results in an increase in bone fragility and a greater tendency to fractures. The loss of bone mass and the deterioration of the microarchitecture are consequences of an alteration in the phenomenon of bone renewal, whose fundamental protagonist is what is called a “unit of bone remodelling”. Osteoporosis is therefore, ultimately nothing but a functional alteration in this unit.
Subsequent to the NIH definition, it has been felt necessary to introduce a new concept, that of bone quality2, which was not reflected in it. This concept includes both those aspects related to bone structure as well as those related to the characteristics of bone tissue (intrinsic properties of bone material). It is possible that an alteration in the quality of bone material is involved in the tendency to osteoporotic fractures, but in general its importance –in relation to bone mass and to those structural aspects– is less. Thus it can be accepted that the definition indicated earlier continues to be valid.
The skeleton is an organ of support, and as such it is exposed to the processes of deterioration which all structures which have to bear mechanical load suffer. But differently from inert support structures (columns, beams, etc), bone is a living organ, with capacity for renewal, and for maintaining its conditions of resistance. This renewal takes place in a permanently and has been given the name “bone remodelling”3,4. The speed at which it occurs is known as “bone turnover”.read more
Nowadays there are many therapeutic options available for the treatment of osteoporosis. The objective of this treatment is to reduce the risk of fractures, both vertebral and non-vertebral. Fractures due to osteoporosis bring with them a high level of morbid-mortality1, as well as the social and health costs they carry. In clinical trials the principal parameter for the measurement of the efficacy of treatment of osteoporosis is the reduction in risk of fracture. However, in clinical practice, a follow up after treatment is carried out with a series of measurements of bone mineral density (BMD). Although there is a clear relationship between BMD and the risk of fracture in patients without treatment, this correlation is not so clear in treated patients2. This is important because it should not be forgotten that the objective of treatment for osteoporosis is the reduction in fractures independently of any modification in BMD. This, although it may be an objective parameter for evaluating the response to treatment, never should be its aim.
Among the many therapeutic options teriparatide, or human recombinant PTH (1-34), has an outstanding position. It is classified in the group of bone forming or anabolic drugs in counterpoint to those called anticatabolics or antiresorptives3. It is administered as a daily self-administered subcutaneous injection, with an easily used preloaded pen, and induces the formation of new bone, increasing the rate of bone remodelling in favour of formation, with an increase in trabecular connectivity and thickening of the cortical bone4. Teriparatide improves the mechanical properties of bone5, giving as a result a significant reduction in vertebral and non-vertebral fractures in postmenopausal women with osteoporosis6, in men, and in those with corticoid osteoporosis7,8. It is for this reason that its use is considered appropriate fundamentally in patients at high risk of fracture and for those in whom there has been earlier failed treatment9
Since the initial description of postmenopausal osteporosis in 1941, Osteoporosis (OP) has been considered a disease which appears in women. However, since a few years ago, it has been recognised that OP in men represents a significant problem in public health, since a seventh of vertebral fractures and a fourth to a fifth of all fractures of the hip occur in males, causing significant morbid-mortality1.
Epidemiology of male osteoporosis
There are not many works on the prevalence of male osteoporosis in different populations. It is calculated that some 2 million American males may have OP and that it will increase 20% by 2015. In our experience, the percentage of densitometric OP in the Spanish male population is 4.15% (2.99%-5.31%), which would suppose that there would currently be between 418,000 and 743,000 Spanish males affected2.
Incidence and prevalence of fractures in men
Incidence of hip fractures
The proportion of hip fractures in the male population represents 30% of all hip fractures in the world3. The life risk for hip fractures in men is 6% at the age of 50 years. In 1996 there were 80,000 hip fractures in American men. For the year 2025 an increase in these figures is foreseen.
The MEDOS (Mediterranean Osteoporosis Study) study4, carried out in the Mediterranean basin, and in which this country participated, it was observed that the incidence of hip fracture due to OP in individuals of more than 45 or 50 years, varied in the case of men, between 50 and 100 cases per 100,000 inhabitants per year. In our country it has been estimated that the incidence of hip fractures in those older than 50 years varies between the 127.8/100,000/year of Gran Canaria and the 267.7/100,000/year of Valladolid5, with a female/male ratio of between 2.5-3 to 1.
The morbid-mortality of hip fractures is greater in men than in women. 36% of men with hip fractures die in the year following the fracture6.
The adverse effects of glucocorticoids (GC) on the skeleton have been known since Cushing’s description in 1932, who observed the decalcification which accompanied suprarenal hyperplasmia due to a hypophysary adenoma which produces adrenocortitropic hormone1. The wide use nowadays of these drugs has made osteoporosis induced by glucocorticoids (OIC) the most frequent cause of osteoporosis associated with drugs2, constituting, therefore, a health problem of great magnitude. So, for example, it has been estimated that 0.5% of the general population, and 1.7% of women over 55 years receive oral steroids3. This means, paradoxically, that, given that we now have the necessary means for the diagnosis and prevention of OIC, fewer than 14% of patients according to some series3, and 7% according to others4, receive any type of treatment to avoid the loss of bone mass when they are prescribed GC orally. The recognition of this problem and early action are fundamental, given the deleterious consequences of the GCs on bone5-8.
Given the characteristics of this monograph and the limitations of space, we focus, in this chapter, on the effect of the oral corticoids, not including inhaled steroids, on bone mineral metabolism.